Thermo Fisher Scientific Complement Factor Bb Neoantigen Monoclonal Antibody (032B-22.1.X)

Applications

Tested Dilution

Publications

ELISA (ELISA)

Assay-dependent

-

Product Specifications

Species Reactivity

Human

Host/Isotype

Mouse / IgG2a

Class

Monoclonal

Type

Antibody

Clone

032B-22.1.X

Immunogen

Purified Human factor B if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:Complement Factor Bb Neoantigen,uniProtId:P00751-1,ncbiNodeId:9606,antigenRange:1-764,antigenLength:764,antigenImageFileName:MA5-28084_Complement_Factor_Bb_Neoantigen_P00751-1_House_mouse.svg,antigenImageFileNamePDP:MA5-28084_Complement_Factor_Bb_Neoantigen_P00751-1_House_mouse_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

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Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1.125 mg/mL

Purification

Protein A

Storage buffer

BBS

Contains

<0.1% sodium azide

Storage conditions

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

Shipping conditions

Wet ice

RRID

AB_2745074

Product Specific Information

This antibody recognizes a neoantigen of the Bb fragment of human complement factor B. Factor B is present in blood serum. C3b associates with complement factor B, inducing conformational change. This enables complement factor D to cleave the N-terminal of complement factor B (the Ba subunit) leaving the 63 kDa Bb subunit associated with C3b and forming C3 convertase. Subunit Bb is involved in the proliferation of preactivated B lymphocytes. Conversely, Ba inhibits lymphocyte proliferation.

Target Information

CFB is involved in hemolytic uremic syndrome atypical 4 (AHUS4), an atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Disease susceptibility is associated with variations affecting the gene represented in this entry. Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.